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Ameliorative effect of vanadium on oxidative stress in stomach tissue of diabetic rats.


Diabetes mellitus is a metabolic disorder characterized by hyperglycemia and insufficency of secretion or action of endogenous insulin. While exogenous insulin and other medications can control many aspects of diabetes, numerous complications affecting several tissues are common and are extremely costly in terms of longevity and quality of life [1]. Increasing evidence in experimental and clinical studies suggests that oxidative stress plays a major role in the pathogenesis of both types of diabetes mellitus. Free radicals are formed disproportionately in diabetes by glucose oxidation, non-enzymatic glycation of proteins and subsequent oxidative degradation of glycated proteins. Abnormally high levels of free radicals and the simultaneous decline of antioxidant defense mechanisms can lead to damage of cellular organelles, increased lipid peroxidation and development of insulin resistance. The consequences of oxidative stress can promote the development of complications of diabetes mellitus [1]. The oxidative effect of diabetes on stomach tissue is demonstrated by the impairment of some biochemical parameters [2-4]. Vanadium derivatives have been shown to possess insulin mimetic and antidiabetic activities in animal models of type 1 and type 2 diabetes mellitus as well as in a small number of diabetic human subjects [5-8]. However, despite numerous studies during the past decade, the mechanism(s) by which vanadium mediates its in vivo antidiabetic effects are not well understood [9]. In a review, on considering the effects of vanadium on carbohydrate and lipid metabolisms, Cam et al. [10] concluded that vanadium acts selectively and by enhancing rather than by mimicking the effects of insulin in vivo. There are also different views on the efficacy of vanadium in the control of hyperglycaemia. Smith et al. [11] states that there is no rigorous evidence that oral vanadium supplementation improves glycaemic control in type 2 diabetes and that the routine use of vanadium for this purpose cannot be recomended. On the other hand, numerous studies report the glucose lowering effect of vanadium salts and propose vanadium complexes as potential agents in the aid of glycaemic control [12-15]. As a result of its more common occurrence in the environment, vanadium is absorbed by plants and travels along the food chain into the body of animals and humans. Although there is no strong evidence that vanadium is an essential trace element for human, a necessary dose of 10 [micro]g/ daily in humans is reported [16]. There are contradictory reports on whether vanadium compounds have toxic effects or not. Domingo et al. [17] reported severe toxic side effects of vanadium on streptozotocin-induced diabetic rats, while Dai et al. [18] concluded that vanadyl sulphate at antidiabetic doses is not significantly toxic to rats following a one-year administration. It is known that vanadium is poorly absorbed in the gastrointestinal tract and rapidly excreted by kidneys [19] which reduces its toxic effects and accumulation in tissues, but also limits its therapeutic efficacy. The accumulation of vanadium in tissues follows the order; bone > kidney > liver > spleen > intestines > stomach > muscle > testis > lung > brain [20]. For several years inorganic vanadium compounds, such as sodium orthovanadate and vanadyl sulfate were used in both animal and human studies. Although these compounds were shown to be glucose-lowering agents, their side effects, mainly gastrointestinal discomfort [13], limited their use as therapeutic agents [9]. In this study, the ameliorative potential of oral administration of vanadium on the stomach tissue of streptozotocin (STZ)-diabetic rats via its effect on antioxidant system enzymes was investigated in order to elucidate the mechanism by which this trace element exerts its beneficial effects.


Animals and treatment

The experiments were reviewed and approved by the Animal Care and Use Institute Committee of Istanbul University. In this study, 6-6.5 months old male Swiss albino rats were used. Animals were acclimatized to their environment for one week prior to experimentation. The animals were housed in a room with a 12 h light/dark cycle at about 22[degrees]C and fed on standard diet with ad libitum access to drinking water. The rats were randomly divided into 4 groups: Control: non-diabetic intact animals (n=13), Control+Va: control animals given vanadyl sulfate (n=5), Diabetic: STZ-diabetic untreated animals (n=n), Diabetic+Va: STZ-diabetic animals treated with vanadyl sulfate (n=n). Diabetes was induced by intraperitoneal injection of STZ in a single dose of 65 mg/kg body weight. STZ was dissolved in a freshly prepared 0.01 M citrate buffer (pH 4.5). Vanadyl sulfate was given by gavage at a dose of 100 mg/kg body weight daily for 60 days. The body weight of all rats was measured at days 0, 1, 30 and 60 [12]. At the last day of the experiment (60th day), rats were sacrificed, stomach tissue was taken and homogenized by means of a glass homogenizer in cold saline to make a 10% (w/v) homogenate.

Biochemical assays

After STZ injections, blood samples of the rats were collected from the tail vein at days 0, 1, 30 and 60. Blood glucose levels after 18 h fasting were measured [21]. The enzyme activities such as catalase (CAT), superoxide dismutase (SOD), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione-S-transferase (GST), myeloperoxidase (MPO), carbonic anhydrase (CA), glucose-6-phosphate dehydrogenase (G6PD) and lactate dehydrogenase (LDH) were assayed in appropriately diluted stomach tissue homogenates. CAT activity was assayed by measuring the decomposition rate of [H.sub.2][O.sub.2] and the enzyme activity was expressed [micro]mol [H.sub.2][O.sub.2] consumed/min/mg protein [22]. SOD activity was assayed by its ability to increase the rate of riboflavin-sensitized photo-oxidation of o-dianisidine according to the method described by Mylroie et al. [23]. The enzyme activity was calculated using bovine erythrocyte SOD as standard and expressed as unit/mg protein. GR [24] and GPx [25] activities were monitored by following the oxidation of NADPH and the enzyme activity was expressed as [micro]mol NADPH oxidized/min/mg protein. GST activity was measured using 1-chloro-2,4-dinitrobenzene (CDNB) as a substrate by the method of Habig and Jacoby [26]. The method is based on the determination of the rate of conjugate formation between glutathione and CDNB. The enzyme activity was expressed as [micro]mol CDNB conjugate formed/min/mg protein. MPO activity was measured according to Hillegass et al. [27]. One unit of the enzyme activity was defined as the amount of MPO required to decompose 1 [micro]mole of [H.sub.2][O.sub.2] in 1 min and the results were expressed as unit/mg protein. CA activity was determined using p-nitrophenyl acetate as a substrate and the enzyme activity was defined as [micro]mol 4-nitrophenol formed/ min/mg protein [28]. G6PD activity was assayed by monitoring the NADPH production at 340 nm and the enzyme activity was expressed as [micro]mol [NADP.sup.+] reduced/min/mg protein [29]. LDH activity was determined by the method of Moss and Henderson [30]. In this method NADH oxidation was monitored by the decrease in absorbance at 340 nm and the enzyme activity was defined as [micro]mol NADH oxidized/min/ mg protein. Total protein content was assayed by the method of Lowry et al. [31], using bovine serum albumin as a standard.

Statistical analysis

The results were given as mean [+ or -] SD and evaluated parametrically using an unpaired t-test and ANOVA variance analysis with the NCSS statistical computer package. p < 0.05 value was considered significant.


The baseline characteristics of the rats, concerning body weights (g) and fasting blood glucose levels (mmol/L) were shown in Table 1. and Table 2., respectively. The effects of vanadium on oxidative stress parameters in stomach tissue were presented in Table 3. In the diabetic group, SOD (p < 0.05), GR (p < 0.001), GPx (p < 0.05), GST (p < 0.05), CA (p < 0.05), G6PD (p < 0.001) and LDH (p < 0.05) activities significantly but CAT activity insignificantly increased in stomach tissue when compared to the control group. Vanadium supplementation to the diabetic rats significantly (p < 0.05) reduced the elevated activities of GR, GPx, GST compared with the diabetic group whereas the decreases in CAT, SOD, CA, G6PD and LDH activities were insignificant. No significant change was seen for MPO activity between the groups. It was observed that vanadyl sulfate had no significant toxic effect on stomach tissue enzymes tested as seen in the group which was treated with vanadyl sulfate alone (Control+Va) when compared to the control group.


It is believed that oxidative stress plays an important role in diabetes and that the management of this phenomenon can be important in dealing with diabetic complications. In this case, vanadyl sulfate was chosen as supplement due to its known beneficial effect on diabetes. But some toxic effects of vanadium due to its accumulation in tissues are raising some questions in view of its use as alternative therapy. The present study was undertaken in order to assess the antioxidant potential of vanadium and to see whether it has any toxic effect on stomach tissue of diabetic rats or not. In a previous study the levels of lipid peroxidation and non-enzymatic glycosylation increased whereas glutathione decreased, representing increased utilization due to oxidative stress, which were reversed by the administration of vanadyl sulfate in stomach tissue of STZ-diabetic animals [32]. In the fight against oxidative stress, SOD turns the superoxide radical to hydrogen peroxide which in turn is converted to water by CAT/GPx [33]. Thus, impairment (which could be increase or decrease) in enzyme levels is accepted as marker for oxidative stress. In the present study CAT and SOD levels increased in the stomach tissue of diabetic rats due to the need for antioxidant defense, and vanadium supplementation restored the impaired enzyme levels, showing its beneficial effect. GPx has been shown to be important in increased peroxidative stress [34]. In our study a significant increase in GPx and GR activities was found which confirms an efficacious defense of the diabetic stomach against oxidative stress. The data obtained were similar to those presented by Gumieniczek et al. [35] for the diabetic heart. In agreement with our previous study [36] vanadyl sulfate restored the increased levels of GR and GPx showing its protective effect. Similarly, impairment in CAT, SOD, GR and GPx activities in stomach of STZ-diabetic animals was recently reported [3]. GST is a group of multifunctional detoxification enzymes, and the expression of the enzyme is affected by oxidative stress, usually observed in diabetes [37]. In the stomach tissue, the significant raise in GST levels in the diabetic group was returned to nearly normal control group levels, proving the antioxidant effect of vanadium. MPO is a hemoperoxidase released by polimorphnuclear neutrophils which catalyzes the formation of numerous ROS, thus has strong proinflammatory and pro-oxidative properties [38]. No significant change was found for MPO activity between the groups suggesting that this mechanism was not involved in this case. CA is a class of zinc metalloenzymes that reversibly catalyzes hydration of carbon dioxide to bicarbonate and a proton [39]. CA isoenzymes have also been shown to be overexpressed in the cellular response to oxidative stress [40]. In the present study, we found that there was an increase in CA activity in the stomach tissue of the diabetic rats, in accordance with our previous studies [21, 41]. Administration of vanadium provoked a decrease in CA activity, however the difference was not significant. G6PD is the principle source of NADPH which is of central importance to cellular redox regulation and any changes in G6PD will alter NADPH levels, thus impact the entire antioxidant system and makes tissues very vulnerable to oxidative damage [42]. Significantly increased activity of G6PD was observed in stomach tissue of diabetic rats, however vanadium supplemention did not alter the enzyme activity showing that vanadium does not interfere with this key enzyme of carbohydrate metabolism. According to Ainscow et al. [43] overexpression of LDH activity may be directly responsible for insulin secretory defect in some forms of diabetes. Increased LDH activity in diabetic rats has also been reported by various researchers [44-46]. Similarly, in this study an increase in the activity of LDH was observed in the stomach tissue of diabetic rats which was slightly reduced by vanadium treatment.


This study has demonstrated that administration of vanadium at a dose of 100 mg/kg body weight showed ameliorative effect against oxidative stress in the stomach tissues of STZ-diabetic rats. Thus, we suggest that this trace element could be used as antioxidant in diabetic complications.


The authors declare that there is no conflict of interest.


This work was supported by Istanbul University Scientific Research Projects. Project Number: UDP-25550.


[1] Maritim AC, Sanders RA, Watkins JB 3rd. Diabetes, oxidative stress, and antioxidants: a review. J Biochem Mol Toxicol 2003; 17(i):24-38.

[2] Pimple BP, Kadam PV, Patil MJ. Protective effect of Luffa acutangula extracts on gastric ulceration in NIDDM rats: role of gastric mucosal glycoproteins and antioxidants. Asian Pac J Trop Med 2012; 5(8): 610-615.

[3] Coskun ZM, Sacan O, Karatug A, Turk N, Yanardag R, Bolkent S, et al. Regulation of oxidative stress and somatostatin, cholecystokinin, apelin gene expressions by ghrelin in stomach of newborn diabetic rats. Acta Histochem 2013; 115(7): 740-747.

[4] Jin QH, Shen HX, Wang H, Shou QY, Liu Q. Curcumin improves expression of SCF/c-kit through attenuating oxidative stress and NF-[kappa]B activation in gastric tissues of diabetic gastroparesis rats. Diabetol Metab Syndr 2013; 5(1): 12.

[5] Thompson KH, McNeill JH, Orvig C. Vanadium compounds as insulin mimics. Chem Rev 1999; 99(9): 2561-2572.

[6] Rehder D. Biological and medicinal aspects of vanadium. Inorg Chem Commun 2003; 6(5): 604-617.

[7] Goldwaser I, Gefel D, Gershonov E, Fridkin M, Shechter Y. Insulin-like effects of vanadium: basic and clinical implications. J Inorg Biochem 2000; 80(1-2): 21-25.

[8] Ramachandran B, Kandaswamy M, Narayanan V, Subramanian S. Insulin mimetic effects of macrocyclic binuclear oxovanadium complexes on streptozotocin-induced experimental diabetes in rats. Diabetes Obes Metab 2003; 5(6): 455-461.

[9] Marzban L, McNeill JH. Insulin-like actions of vanadium: Potential as a therapeutic agent. J Trace Elem Exp Med 2003; 16(4): 253-267.

[10] Cam MC, Brownsey RW, McNeill JH. Mechanisms of vanadium action: insulin-mimetic or insulin-enhancing agent? Can J Physiol Pharmacol 2000; 78(10): 829-847.

[11] Smith DM, Pickering RM, Lewith GT. A systematic review of vanadium oral supplements for glycaemic control in type 2 diabetes mellitus. QJM 2008; 101(5): 351-358.

[12] Bolkent S, Bolkent S, Yanardag R, Tunali S. Protective effect of vanadyl sulfate on the pancreas of streptozotocin-induced diabetic rats. Diabetes Res Clin Pract 2005; 70(2): 103-109.

[13] Srivastava AK. Anti-diabetic and toxic effects of vanadium compounds. Mol Cell Biochem 2000; 206(1-2): 177-182.

[14] Badmaev V, Prakash S, Majeed M. Vanadium: a review of its potential role in the fight against diabetes. J Altern Complement Med 1999; 5(3): 273-291.

[15] Poucheret P, Verma S, Grynpas MD, McNeill JH. Vanadium and diabetes. Mol Cell Biochem 1998; 188(1-2): 73-80.

[16] Goc A. Biological activity of vanadium compounds. Cent Eur J Biol 2006; 1(3): 314-332.

[17] Domingo JL, Gomez M, Llobet JM, Corbella J, Keen CL. Oral vanadium administration to streptozotocin-diabetic rats has marked negative side-effects which are independent of the form of vanadium used. Toxicology 1991; 66(3): 279-287.

[18] Dai S, Thompson KH, Vera E, McNeill JH. Toxicity studies on one-year treatment of non-diabetic and streptozotocin-diabetic rats with vanadyl sulphate. Pharmacol Toxicol 1994; 75(3-4): 265-273.

[19] Barceloux DG. Vanadium. J Toxicol Clin Toxicol 1999; 37(2): 265-278.

[20] Sharma RP, Oberg SG, Parker RD. Vanadium retention in rat tissues following acute exposures to different dose levels. J Toxicol Environ Health 1980; 6(1): 45-54.

[21] Koyuturk M, Tunali S, Bolkent S, Yanardag R. Effects of vanadyl sulfate on liver of streptozotocin-induced diabetic rats. Biol Trace Elem Res 2005; 104(3): 233-247.

[22] Aebi H. Catalase in vitro. Methods Enzymol 1984; 105: 121-126.

[23] Mylroie AA, Collins H, Umbles C, Kyle J. Erythrocyte superoxide dismutase activity and other parameters of copper status in rats ingesting lead acetate. Toxicol Appl Pharmacol 1986; 82(3): 512-520.

[24] Carlberg I, Mannervik B. Glutathione reductase. Methods Enzymol 1985; 113: 484-490.

[25] Lawrence RA, Burk RF. Glutathione peroxidase activity in selenium-deficient rat liver. Biochem Biophys Res Commun 1976; 71(4): 952-958.

[26] Habig WH, Jakoby WB. Assays for differentiation of glutathione-S-transferases. Methods Enzymol 1981; 77: 398-405.

[27] Hillegass LM, Griswold DE, Brickson B, Albrightson-Winslow C. Assessment of myeloperoxidase activity in whole rat kidney. J Pharmacol Methods 1990; 24(4): 285-295.

[28] Verpoorte JA, Mehta S, Edsall JT. Esterase activities of human carbonic anhydrases B and C. J Biol Chem 1967; 242(18): 4221-4229.

[29] Betke K, Brewer GJ, Kirkman HN, Luzzato L, Motulsky AG, Ramot B, et al. Standardized method for G-6-PD assay of haemolysates. WHO Tech Rep Ser 1967; 366: 30-32.

[30] Moss DW, Henderson AR. Enzymes. In; Burtis CA, Ashwood ER (eds.). Tietz textbook of clinical chemistry, 2nd edn. Philadelphia: WB Saunders; 1994, pp. 816-818.

[31] Lowry OH, Rosebrough NJ, Farr AL, Randall RJ. Protein measurement with the Folin phenol reagent. J Biol Chem 1951; 193(1): 265275.

[32] Tunali S, Yanardag R. Effect of vanadyl sulfate on the status of lipid parameters and stomach and spleen tissues of streptozotocin-induced diabetic rats. Pharmacol Res 2006; 53(3): 271-277.

[33] Singh N, Kamath V, Narasimhamurthy K, Rajini PS. Protective effect of potato peel extract against carbon tetrachloride-induced liver injury in rats. Environ Toxicol Pharmacol 2008; 26(2): 241-246.

[34] Matkovics B, Varga SI, Szabo L, Witas H. The effect of diabetes on the activities of the peroxide metabolism enzymes. Horm Metab Res 1982; 14(2): 77-79.

[35] Gumieniczek A, Hopkala H, Wojtowicz Z, Nikolajuk J. Changes in antioxidant status of heart muscle tissue in experimental diabetes in rabbits. Acta Biochim Pol 2002; 49(2): 529-535.

[36] Kurt O, Ozden TY, Ozsoy N, Tunali S, Can A, Akev N, et al. Influence of vanadium supplementation on oxidative stress factors in the muscle of STZ-diabetic rats. Biometals 2011; 24(5): 943-949.

[37] Wang G, Zhang L, Li Q. Genetic polymorphisms of GSTT1, GSTM1, and NQO1 genes and diabetes mellitus risk in Chinese population. Biochem Biophys Res Commun 2006; 341(2): 310-313.

[38] Roman RM, Wendland AE, Polanczyk CA. Myeloperoxidase and coronary arterial disease: from research to clinical practice. Arq Bras Cardiol 2008; 91(1): e11-e19.

[39] Zimmerman UJ, Wang P, Zhang X, Bogdanovich S, Forster R. Anti-oxidative response of carbonic anhydrase III in skeletal muscle. IUBMB Life 2004; 56(6): 343-347.

[40] Raisanen SR, Lehenkari P, Tasanen M, Rahkila P, Harkonen PL, Vaananen HK. Carbonic anhydrase III protects cells from hydrogen peroxide-induced apoptosis. FASEB J 1999; 13(3): 513-22.

[41] Yilmaz-Ozden T, Kurt-Sirin O, Tunali S, Akev N, Can A, Yanardag R. Effect of oral vanadium supplementation on oxidative stress factors in the lung tissue of diabetic rats. Trace Elem Electrolytes 2014; 31(2): 48-52.

[42] Shailey S, Basir SF. Strengthening of antioxidant defense by Azadirachta indica in alloxan-diabetic rat tissues. J Ayurveda Integr Med 2012; 3(3): 130-135.

[43] Ainscow EK, Zhao C, Rutter GA. Acute overexpression of lactate dehydrogenase-A perturbs beta-cell mitochondrial metabolism and insulin secretion. Diabetes 2000; 49(7): 1149-1155.

[44] Palsamy P, Subramanian S. Modulatory effects of resveratrol on attenuating the key enzymes activities of carbohydrate metabolism in streptozotocin-nicotinamide-induced diabetic rats. Chem Biol Interact 2009; 179(2-3): 356-362.

[45] Farswan M, Mazumder PM, Percha V. Protective effect of Cassia glauca Linn. on the serum glucose and hepatic enzymes level in streptozotocin induced NIDDM in rats. Indian J Pharmacol 2009; 41(1): 19-22.

[46] Patel SS, Goyal RK. Prevention of diabetes-induced myocardial dysfunction in rats using the juice of the Emblica officinalis fruit. Exp Clin Cardiol 2011; 16(3): 87-91.

Tugba Yilmaz-Ozden (1) *, Ozlem Kurt-Sirin (1), Sevim Tunali (2), Nuriye Akev (1), Ayse Can (1), Refiye Yanardag (2)

(1) Department of Biochemistry, Faculty of Pharmacy, Istanbul University, Beyazit, 34116, Istanbul, Turkey. (2) Department of Chemistry, Faculty of Engineering, Istanbul University, Avcilar, 34320, Istanbul, Turkey.

* Corresponding author: Tugba Yilmaz-Ozden, Department of Biochemistry, Faculty of Pharmacy, Istanbul University, Beyazit, 34116, Istanbul, Turkey Phone: +90 212 4400000/13411 Fax: +90 212 4400252


Submitted: 28 November 2013/Accepted: 16 April 2014
TABLE 1. Mean levels of weight parameters (g) for all groups [12].

Group                   0 Day                   1 Day

Control         246.64 [+ or -] 44.43   243.35 [+ or -] 39.50
Control+Va      224.17 [+ or -] 16.13   221.03 [+ or -] 12.58
Diabetic        231.67 [+ or -] 37.71   197.02 [+ or -] 37.47
Diabetic+Va     229.65 [+ or -] 32.14   203.93 [+ or -] 30.57
[P.sub.ANOVA]           0.571                   0.011

Group                  30 Day                  60 Day

Control         275.51 [+ or -] 34.40   283.48 [+ or -] 30.35
Control+Va      253.14 [+ or -] 14.06   251.91 [+ or -] 20.41
Diabetic        175.74 [+ or -] 38.48   171.70 [+ or -] 34.67
Diabetic+Va     197.46 [+ or -] 34.40   199.16 [+ or -] 36.20
[P.sub.ANOVA]          0.0001                  0.0001

The values were given as mean [+ or -] SD.

TABLE 2. Mean levels of blood glucose (mmol/L) for all groups [21].

Group                 0 Day                 1 Day

Control         4.14 [+ or -] 0.82   4.34 [+ or -] 0.71
Control+Va      4.05 [+ or -] 0.52   4.72 [+ or -] 1.07
Diabetic        3.64 [+ or -] 0.32   11.75 [+ or -] 2.39
Diabetic+Va     3.99 [+ or -] 0.76   14.09 [+ or -] 2.14
[P.sub.ANOVA]         0.324                0.0001

Group                 30 Day                60 Day

Control         4.49 [+ or -] 0.74    3.83 [+ or -] 0.51
Control+Va      4.22 [+ or -] 0.90    4.80 [+ or -] 0.61
Diabetic        12.03 [+ or -] 2.03   17.95 [+ or -] 7.29
Diabetic+Va     7.54 [+ or -] 2.56    7.31 [+ or -] 4.01
[P.sub.ANOVA]         0.0001                0.0001

The values were given as mean [+ or -] SD.

TABLE 3. Effect of vanadium supplementation on oxidative stress
parameters in stomach tissue of STZ-diabetic rats

Group                 CAT                   SOD

Control         4.8 [+ or -] 1.4     0.32 [+ or -] 0.09
Control+Va      4.4 [+ or -] 1.3     0.26 [+ or -] 0.04
Diabetic        5.2 [+ or -] 2.0   0.51 [+ or -] 0.04 (a)
Diabetic+Va     3.8 [+ or -] 1.1     0.45 [+ or -] 0.04
[P.sub.ANOVA]        0.309                 0.001

Group                    GR                       GPx

Control           4.3 [+ or -] 0.9        441.1 [+ or -] 147.4
Control+Va        6.3 [+ or -] 0.3        347.8 [+ or -] 109.0
Diabetic        13.5 [+ or -] 1.4 (b)   680.1 [+ or -] 182.1 (a)
Diabetic+Va     10.0 [+ or -] 2.5 (c)   450.5 [+ or -] 107.4 (c)
[P.sub.ANOVA]          0.0001                    0.0001

Group                    GST                    MPO

Control           65.6 [+ or -] 12.9     0.03 [+ or -] 0.01
Control+Va        61.5 [+ or -] 15.3     0.04 [+ or -] 0.02
Diabetic        89.4 [+ or -] 23.0 (a)   0.03 [+ or -] 0.01
Diabetic+Va     62.6 [+ or -] 11.5 (c)   0.03 [+ or -] 0.01
[P.sub.ANOVA]           0.008                  0.925

Group                    CA                     G6PD

Control           1.6 [+ or -] 0.3       0.02 [+ or -] 0.01
Control+Va        1.6 [+ or -] 0.4       0.01 [+ or -] 0.01
Diabetic        2.1 [+ or -] 0.5 (a)   0.05 [+ or -] 0.01 (b)
Diabetic+Va       1.7 [+ or -] 0.5       0.04 [+ or -] 0.01
[P.sub.ANOVA]          0.149                   0.0001

Group                    LDH

Control           13.3 [+ or -] 4.5
Control+Va        11.7 [+ or -] 3.9
Diabetic        28.3 [+ or -] 13.8 (a)
Diabetic+Va       14.3 [+ or -] 7.5
[P.sub.ANOVA]           0.016

The values were given as mean [+ or -] SD.

(a) p < 0.05 versus Control; (b) p < 0.001 versus Control;
(c) p < 0.05 versus Diabetic. All enzyme activities were
expressed as unit/mg protein.
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Author:Yilmaz-Ozden, Tugba; Kurt-Sirin, Ozlem; Tunali, Sevim; Akev, Nuriye; Can, Ayse; Yanardag, Refiye
Publication:Bosnian Journal of Basic Medical Sciences
Article Type:Report
Geographic Code:4EXBO
Date:May 1, 2014
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